Sleep apnea is defined as cessation of breathing during sleep lasting at least 10 seconds and is classified as obstructive or central. Obstructive sleep apnea is caused by intermittent upper airway obstruction while central involves impaired respiratory drive. Sleep apnea is common, affecting 9% of women and 24% of men, and is associated with increased morbidity and mortality if left untreated. Treatment depends on severity but often involves continuous positive airway pressure.

1. SLEEP APNEA

2. • Sleep apnea is defined as the cessation of airflow
at the nose andvmouth lasting at least 10
seconds.
• Sleep apnea is quantified using polysomnography
(PSG) and is classified into two major categories:
• obstructive and central.
• Central sleep apnea involves impairment of the
respiratory drive, while obstructive sleep apnea is
caused by intermittent upper airway obstruction.

3. • Some patients will experience both central
and obstructive sleep apnea.
• Patients with this sleep disorder have a high
risk of morbidity and mortality

4. • Sleep apnea is very common. Approximately 9%
of females and 24% of males experience sleep
apnea.
• Sleep apnea is two to three times more common
in men, and it is more common in middle-aged
men than in younger men.
• As many as 80% of middle-aged men snore, and
25% of heavy snorers have sleep apnea.
• Sleep apnea may be less prevalent in elderly
patients, and it is theorized that this may be
evidenced by sleep apnea’s effect on mortality

5. OBSTRUCTIVE SLEEP APNEA
• Obstructive sleep apnea (OSA) is a potentially life-threatening
condition characterized by snoring.
• At one end of the spectrum are those individuals
who snore intermittently with little sleep
disruption, and at the other end are patients who
snore heavily and have severe gas exchange
disturbances and respiratory failure, causing
them to gasp for air.
• These episodes are repeated as often as 600
times per night.

6. • As a result of these frequent arousals, hypoxia
and sleep fragmentation occur.
• Hypoxia may lead to daytime sleepiness,
impaired attention and memory, and
personality changes.
• Individuals with sleep apnea are usually not
aware of the snoring or respiratory pauses,
and symptoms are most frequently reported
by their bed partner.

7. • OSA is caused by occlusion of the upper airway
due to factors such as obesity, and fixed upper
airway lesions such as polyps, as well as enlarged
tonsils or adenoids or the tongue.
• It can also be caused by acromegaly, amyloidosis,
and hypothyroidism, as well as neurological
conditions that impair upper airway muscle tone.
• Medical complications include arrhythmias,
hypertension, cor pulmonale, and sudden death.

8. • Treatment of OSA must be individualized and depends
on the severity of the disordered breathing and the
amount of sleep disruption.
• Patients with severe apnea (>20 episodes per hour on
PSG and excessive daytime somnolence) and those
with moderate apneas (5 to 20 episodes per hour on
PSG and excessive daytime somnolence or other
daytime symptoms) have shown significant
improvement and reduction in mortality with
treatment.
• Nonpharmacologic measures are the treatments of
choice.

9. • Weight loss may eliminate the apnea and reduce
daytime hypersomnia; however, improvement is
only limited.
• Treatment of underlying causes of obstruction
(e.g., tonsillectomy, nasal septal repair, and
nonsedating antihistamines for allergic rhinitis)
may eliminate apneas during sleep.
• In patients with mild apnea and snoring with no
daytime symptomatology, management may
include avoidance of a supine sleep position.

10. • Continuous positive airway pressure (CPAP)
during sleep is the standard treatment for most
patients with OSA.
• CPAP acts as a splint to maintain the patency of
the oropharynx during respiration.
• Compliance is variable, ranging from 25% to 70%,
and is the major limitationof this treatment.
• One night of noncompliance results in a complete
reversal of the gains made in daytime alertness

11. • The most important pharmacologic
intervention is the avoidance of all CNS
depressants (e.g., alcohol, anxiolytics,
hypnotics, narcotics, and zolpidem).
• Preliminary studies suggest that zaleplon does
not interfere with respiratory function.
• CNS depressant use is potentially lethal since
it inhibits the brain’s reflex ability to cause a
mini-arousal and resume breathing

12. • Medication therapy should be reserved for
patients with mild OSA and those who are
treatment resistant.
• Protriptyline in doses of 10 to 30 mg daily
reduces the frequency of apneas and
increases oxygen saturation.

13. • The mechanism of action may be related to a
decrease in REM sleep, the sleep stage in
which most apneas occur.
• Imipramine was found to exert similar effects
to protriptyline in two uncontrolled studies.
• Fluoxetine and paroxetine have shown results
similar to those of protriptyline, with fewer
adverse effects.

14. • The SSRIs may be preferable to tricyclic
antidepressants due to their similar efficacy but
fewer adverse effects.
• Medroxyprogesterone (MPG) has proved
disappointing in OSA, showing no results in curing
nighttime apnea.
• In contrast, MPG does appear to have a beneficial
effect in daytime hypercapnia.
• At present the only role for MPG is in OSA
patients with awake respiratory failure or
noncompliance with CPAP.

15. • Theophylline is a respiratory stimulant that has
been frequently used in patients with OSA.
• Studies with theophylline have shown
questionable efficacy.
• Some studies have shown a reduction in
obstructive events, but an increase in the number
of arousals, increasing daytime sleepiness.
• Mixed reviews have also been found for
antihypertensive agents.

16. • Studies have evaluated the effects of
angiotensin-converting enzyme inhibitors,
calcium channel blockers, metoprolol, and
clonidine, showing reduction in the frequency
of apnea.
• Studies have also shown that
antihypertensives can increase OSA.
• Thus the efficacy of these agents is unclear.

17. CENTRAL SLEEP APNEA
• Central sleep apnea (CSA) is a form of apnea in
which breathing effort is not detected, in contrast
to obstructive apnea, in which attempts at
breathing are vigorous.
• CSA makes up only 10% of all apneas.
Hypercapnic patients usually present with a
morning headache and daytime somnolence,
while nonhypercapnic patients complain of
insomnia and nocturnal awakenings with
shortness of breath or gasping.

18. • Although the majority of cases are idiopathic,
identifiable causes are nasal obstruction,
autonomic nervous system lesions (e.g.,
cervical cordotomy), neurological diseases
(e.g., poliomyelitis, encephalitis, and
myasthenia gravis), and congestive heart
failure.

19. • The primary treatment approach for CSAis
supplemental oxygen and CPAP.
• Pharmacologic treatments include
acetazolamide, theophylline, and MPG.
• Acetazolamide induces a metabolic acidosis
that stimulates respiratory drive.
• Long-term studies have shown a 70%
reduction in CSA with acetazolamide, and no
effect on obstructed breathing events.

20. • It has been suggested that acetazolamide
induces a resetting of the CO2 response
threshold.
• Clinical use is limited because of adverse
effects such as electrolyte changes,
paresthesias, and precipitation of calcium
phosphate salts in alkaline urine.
• Theophylline may have some efficacy in CSA
related to congestive heart failure.

21. • In one trial there was a 60% reduction in
central apneas per hour of sleep compared
with 20% with placebo,29 but further study is
needed.
• In nonhypercapnic CSA patients, treatment
may consist of benzodiazepines (triazolam or
temazepam) to reduce arousals, and
acetazolamide, CPAP, and oxygen to stabilize
breathing patterns